When EGFR- tyrosine kinase inhibitor (TKI) therapies, such as erlotinib or gefitinib, are used to target EGFR mutations in NSCLC, cells with MET amplification can bypass the blocked EGFR signaling by activating alternative pathways through MET, leading to continued tumor growth and survival despite EGFR inhibition (19, 20). This evidence concerns the gene EGFR and neoplasm.